Biomolecular markers and pulmonary structure in rats exposed to acute intermittent hypobaria

Abstract

Introduction: Intermittent hypobaric hypoxia (IHH) is a new relative form of human exposure to high altitude. In Chile, 60000 workers who live at sea level must shift every 5 or 7 days to work in mining prospecting located over 3000 MASL. Pathophysiological effects of chronic and acute hypobaria in humans have been studied extensively and are closely related to oxidative stress. However, few studies about IHH has been performed, with the lung being one of the most affected and least investigated organs. Hypothesis: Acute IHH will induce the expression and activity of antioxidant enzymes in lung tissue, preserving oxidative tone and pulmonary arteries (AP) morphology relative to normoxic controls. Objective: To determine antioxidant capacity, level of oxidative stress and AP structure in normoxic and AIHH rats. Material and Methods: 12 Wistar adult rats were divided into 2 groups, one was exposed to simulated IHH and other was kept under normobaric conditions. IHH was induced in a hypobaric chamber in 4 continuous cycles (1 cycle = 4 d at 425 mmHg + 4 d at 720 mmHg). Lungs were removed and divided for study. We determined levels of TBARS, Thiolic index, HIF 1-2 α, expression and activity of antioxidant enzymes. Histomorphometry of AP was performed. Results: IHH exposure induced increased CAT and decreased GPx activity. Hypoxia induced a marked increase in oxidative stress markers relative to control animals. Dorsal pulmonary regions showed vascular wall remodeling in small AP compared to control. Conclusion: IHH produced changes in protein expression/activity. Early stages of IHH cycles are detrimental to pulmonary homeostasis. Further studies should evaluate the effects of several IHH shifts.